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滇乌碱通过线粒体凋亡途径致大鼠心肌损伤的研究
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| 篇名： | 滇乌碱通过线粒体凋亡途径致大鼠心肌损伤的研究 |
| TITLE： | Study on myocardial injury of rats induced by yunaconitine through mitochondrial apoptosis pathway |
| 摘要： | 目的 研究滇乌碱对大鼠心肌损伤的影响及其线粒体凋亡途径相关机制。方法采用随机数字表法将40只SD大鼠随机分为正常组（生理盐水），滇乌碱高、低剂量组（0.14、0.09mg/kg），乌头碱组（阳性对照，0.88mg/kg），每组10只，每天灌胃给药1次，连续7d。检测大鼠血清中乳酸脱氢酶（LDH）、肌酸激酶（CK）、肌酸激酶同工酶（CK-MB）、超氧化物歧化酶（SOD）、丙二醛（MDA）水平和心肌组织中活性氧（ROS）水平，观察大鼠心肌组织病理形态学和心肌组织线粒体超微结构变化情况，检测大鼠心肌细胞凋亡情况，检测大鼠心肌组织中B淋巴细胞瘤2（Bcl-2）、Bcl-2相关X蛋白（Bax）、胱天蛋白酶9（caspase-9）、活化的胱天蛋白酶9（cleaved-caspase-9）、caspase-3和cleaved-caspase-3蛋白相对表达水平。结果与正常组比较，滇乌碱高、低剂量组大鼠血清中LDH、CK、CK-MB、MDA水平和心肌细胞凋亡数量及心肌组织中ROS水平、caspase-3蛋白表达水平均显著升高/增加（P＜0.05或P＜0.01），血清中SOD水平和心肌组织中Bcl-2/Bax比值显著降低（P＜0.01），且滇乌碱高剂量组大鼠心肌组织中caspase-9、cleaved-caspase-9、caspase-3、cleaved-caspase-3蛋白相对表达水平显著升高（P＜0.05）；两组大鼠均出现了心肌纤维排列紊乱、线粒体肿胀等病理变化。结论滇乌碱可引起大鼠心肌细胞损伤。其机制可能与破坏心肌细胞膜的完整性，使心肌细胞发生氧化应激，诱导心肌细胞通过线粒体途径发生凋亡有关。 |
| ABSTRACT： | OBJECTIVE To study the effects of yunaconitine on myocardial injury in rats and its mechanism related to mitochondrial apoptosis pathway rats. METHODS Forty SD rats were divided into normal group （normal saline）， yunaconitine high-dose and low-dose groups（0.14， 0.09 mg/kg）and aconitine group （positive control， 0.88 mg/kg） by random number method， with 10 rats in each group. They were given relevant medicine intragastrically， once a day， for consecutive 7 days. The levels of lactate dehydrogenase （LDH）， creatine kinase （CK）， creatine kinase isoenzyme （CK-MB）， superoxide dismutase （SOD） and malondialdehyde （MDA） in serum as well as the level of reactive oxygen species （ROS） in myocardial tissue were detected. The pathomorphological changes of myocardium and ultrastructural changes of myocardial mitochondria were all observed. The apoptosis of cardiomyocytes was determined. The protein relative expressions of B-cell lymphoma-2 （Bcl-2）， Bcl-2 associated X protein （Bax）， caspase-9， cleaved-caspase-9， caspase-3 and cleaved-caspase-3 were determined in myocardium of rats. RESULTS Compared with normal group， the serum levels of LDH， CK， CK-MB and MDA， the apoptotic numbers of cardiomyocytes， the level of ROS and protein expression of caspase-3 in myocardium were increased significantly in yunaconitine high-dose and low- dose groups （P＜0.05 or P＜0.01）； serum level of SOD and Bcl-2/Bax ratio in myocardium were all decreased significantly （P＜ 0.01）； the protein relative expressions of caspase-9， cleaved-caspase-9， caspase-3 and cleaved-caspase-3 in myocardium were significantly increased in yunaconitine high-dose group （P＜0.05）； some pathomorphological changes were found in 2 groups， such as myocardial fiber disorder， mitochondrial swelling. CONCLUSIONS Yunacotine could cause myocardial injury in rats. Its mechanism might be related to destroying the integrity of cardiomyocyte membrane， causing oxidative stress of cardiomyocyte， and inducing the apoptosis of myocardial cells through mitochondrial pathway. |
| 期刊： | 2022年第33卷第23期 |
| 作者： | 司徒莹，程婉秋，沈志滨，陈艳芬，唐春萍，陈聪，江涛 |
| AUTHORS： | SITU Ying，CHENG Wanqiu，SHEN Zhibin，CHEN Yanfen，TANG Chunping，CHEN Cong，JIANG Tao |
| 关键字： | 滇乌碱；心脏毒性；氧化应激；凋亡；线粒体途径；心肌损伤 |
| KEYWORDS： | yunaconitine； cardiotoxicity； oxidative stress； |
| 阅读数： | 191 次 |
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